ObjectiveBased on the clinical characteristics of chronic gouty arthritis （CGA） in both traditional Chinese and western medicine， this study aims to systematically evaluate the clinical concordance of existing CGA animal models， providing recommendations for establishing animal models that align with the pathological characteristics of CGA and the manifestations of traditional Chinese medicine syndromes. MethodsBy comprehensively retrieving Chinese and international databases such as China National Knowledge Infrastructure， Wanfang， VIP Chinese Science and Technology Periodical Database （VIP）， and PubMed， all relevant literature on CGA animal models was collected. Based on the guidelines， the diagnostic criteria of both traditional Chinese and western medicine were summarized and organized. The evaluation indicators for the CGA model were constructed with reference to existing evaluation modes， and the CGA animal models were analyzed to systematically evaluate the clinical concordance of existing models. ResultsThe current methods used to construct CGA animal models mainly include monosodium urate crystal induction， high-protein diet induction （poultry lack urate oxidase）， and high-fat diet combined with urate oxidase inhibitors and joint injection. Based on 11 pieces of included literature， the traditional Chinese and western medicine scoring data of each model were extracted， and the average scoring values of all models were ultimately calculated. The results show that the average clinical concordances of existing CGA animal models in both traditional Chinese and western medicine are 43.33% and 64.44%， respectively. Among them， the model with the highest clinical concordance rate is the one with a high-fat diet combined with potassium oxonate to induce hyperuricemia plus joint injection， achieving 83.33% clinical concordance in western medicine and 60% in traditional Chinese medicine. This model aligns well with the pathogenic characteristics and pathological changes of clinical CGA. ConclusionAlthough current CGA animal models can simulate some pathological characteristics of CGA， they struggle to comprehensively reflect the complex pathological processes of CGA and the characteristics of traditional Chinese medicine syndromes. Therefore， in the future， it is necessary to establish the CGA animal models that incorporate the clinical disease and syndrome characteristics of traditional Chinese and western medicine and formulate the uniform model evaluation criteria， providing more precise tools for CGA mechanism research and the development of traditional Chinese medicine.

ObjectiveTo evaluate the therapeutic effect of Huazhuo SanJie Chubi presciption （HSCD） on chronic gouty arthritis （CGA） rats with low-grade inflammation and to explore the underlying mechanism with a focus on macrophage polarization. MethodsThe 41 male 6-week-old SD rats were randomly allocated， using the random number table， to a normal group （n=8） and a model group （n =33）. CGA with low-grade inflammation was induced in the model group by daily gavage of potassium oxonate （250 mg·kg^-1·d^-1） and hypoxanthine （300 mg·kg^-1·d^-1）， combined with intra-articular injection of a monosodium urate （MSU） crystal suspension （50 μL， 25 g·L^-¹） into the left ankle twice weekly. After 4 weeks of modeling， 3 rats were randomly selected from each group for model validation. The remaining successfully modeled rats were randomly divided into a model group， an HSCD group （10.35 g·kg^-1·d^-1， gavage once daily）， an M1 polarization agonist group （L-methionine sulfoximine， 300 mg·kg^-1， subcutaneous injection every other day）， an M1 polarization agonist + HSCD group， an M2 polarization inhibitor group （PD0325901， 10 mg·kg^-1·d^-1， gavage once daily）， and M2 polarization inhibitor + HSCD group. The corresponding drug or drug combination was administered according to group assignment， whereas rats in the normal and model groups received 0.5% carboxymethyl cellulose sodium （CMC-Na） vehicle （10.35 g·kg^-1·d^-1， gavage once daily）. All interventions were continued for four weeks. During the intervention period， except for the normal group， potassium oxonate （250 mg·kg⁻¹） and hypoxanthine （300 mg·kg^-1） were co-administered by gavage every other day to maintain the model. At the end of treatment， serum uric acid （SUA）， ankle joint diameter and joint swelling index were measured. The levels of high-sensitivity C-reactive protein （hs-CRP）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， chemokine C-C motif ligand 2 （CCL2）， S100 calcium-binding protein A8/A9 （S100A8/A9）， interleukin-10 （IL-10） and arginase-1 （Arg-1） in serum and joint fluid were determined by enzyme-linked immunosorbent assay （ELISA）. High-frequency ultrasound was used to assess MSU deposition in the ankle joint. Hematoxylin-eosin （HE） staining was performed to evaluate synovial histopathological changes. Quantitative Real-time PCR and immunofluorescence were used to detect the mRNA and protein expression of the M1 macrophage polarization markers inducible nitric oxide synthase （iNOS） and the M2 macrophage polarization marker scavenger receptor cysteine-rich type 1 protein M130 （CD163） in synovial tissue. ResultsCompared with the normal group， the model group showed significantly elevated SUA level and joint swelling index， and increased levels of pro-inflammatory cytokines， CCL2， and S100A8/A9 in both serum and joint fluid （P<0.05）， accompanied by MSU deposition and synovial inflammation in the ankle joint. The mRNA and protein expression levels of macrophage polarization M1/M2 markers iNOS and CD163 in synovial tissues were also significantly up-regulated （P<0.05）. Compared with model group， rats in HSCD group had significantly lower SUA levels， attenuated joint swelling， reduced serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in both serum and joint fluid， accompanied with alleviated MSU deposition and synovial inflammation （P<0.05）. HSCD markedly downregulated the mRNA and protein expression of M1 marker iNOS （P<0.05）， whereas it had no significant effect on the expression of M2 marker CD163. Compared with the M1 polarization agonist group， the M1 polarization agonist + HSCD group showed significantly reduced joint swelling， lower serum levels of pro-inflammatory cytokines， and decreased levels of CCL2 and S100A8/A9 in joint fluid （P<0.05）. In addition， synovial inflammatory cell infiltration and angiogenesis were attenuated， and iNOS mRNA and protein expression levels were significantly reduced （P<0.05）. Compared with the M2 polarization inhibitor group， the M2 polarization inhibitor + HSCD group exhibited reduced joint swelling， decreased levels of CCL2 and S100A8/A9 in joint fluid and ameliorated synovial inflammation （P<0.05）， whereas the levels of anti-inflammatory mediators （IL-10， Arg-1） and CD163 mRNA and protein expression were not significantly increased. ConclusionHSCD alleviates low-grade inflammation in CGA rats， at least in part， by inhibiting macrophage polarization toward the M1 phenotype.

Background: and Purpose Live cell-based assays (LCBA) are increasingly used for serological antibody detection due to their ability to preserve antigen conformation, offering moderately higher sensitivity than fixed cell-based assays. However, the clinical necessity of prioritizing LCBA for the detection of aquaporin-4 immunoglobulin G (AQP4-IgG) in neuromyelitis optica spectrum disorder (NMOSD) remains unclear, especially when compared to its established role in diagnosing myelin oligodendrocyte glycoprotein antibody-associated disease. Methods: We compared the performance of live cell-based assays using immunofluorescence (LCBA-IF) and fixed cell-based assays using immunofluorescence (FCBA-IF) in detecting AQP4-IgG in 90 cases of NMOSD meeting 2015 International Panel for Neuromyelitis Optica Diagnosis criteria, alongside 40 controls. Additionally, we further investigated the relationship between AQP4-IgG titers as measured by LCBA-IF and FCBA-IF and clinical parameters in NMOSD patients. Results: Results showed 96.9% agreement between LCBA-IF and FCBA-IF (Cohen’s κ=0.935), with a strong Spearman correlation (0.977, p<0.001). Both methods demonstrated 100% specificity, with LCBA-IF showing slightly higher sensitivity compared to FCBA-IF. Within LCBAIF-tested groups, statistically significant differences in annualized relapse rates were observed across all pairwise comparisons (low-titer vs. moderate-titer, low-titer vs. high-titer, and moderate-titer vs. high-titer; all p<0.050). However, this association reached statistical significance in some FCBA-IF-tested groups. Conclusions Overall, there is a strong concordance between LCBA-IF and FCBA-IF in detecting AQP4-IgG, where LCBA-IF shows slightly higher sensitivity. Furthermore, there is a potential link between elevated AQP4-IgG titers and an increased risk of relapse, and this correlation may appear more pronounced when using LCBA-IF.

BackgroundEmotional disorders in adolescents have emerged as a prominent issue in recent years. Current mainstream clinical assessment approaches for such conditions predominantly rely on interviews and rating scales， which are limited by inherent drawbacks such as high subjectivity and recall bias. Accordingly， there exists an urgent clinical need for the development of objective， quantifiable auxiliary diagnostic tools.In previous studies， frontal electroencephalography （EEG） has demonstrated significant value in assessing depressive and anxiety. However， the lack of standardized quantitative metrics and intuitive visual analytical approaches has severely restricted clinical interpretability of EEG data and diminished patient engagement. To address these key limitations， the present study proposes an innovative analytical framework that converts frontal EEG signals into quantifiable visual metrics to enhance clinical comprehension and acceptance. ObjectiveTo explore the value of frontal EEG in assessing anxiety， depression， and sleep quality in adolescents with emotional disorders， with the aim of providing objective auxiliary tools for clinical diagnosis and assessment of adolescents with emotional disorders. MethodsThis cross-sectional study recruited 105 adolescents aged 12-18 years who visited the outpatient department of a specialized mental hospital in Beijing from April 2023 to April 2024. All participants met the diagnostic criteria for mood （affective） disorders or anxiety disorders in the International Classification of Diseases， tenth edition （ICD-10）. Frontal EEG signals were collected within a big data analytics-driven framework and further processed by EEG system to generate six quantitative cerebral function indices， namely brain load， tension and excitement， emotional stress， sleepiness index， cerebral vitality， and cerebral fatigue. In addition， validated standardized scales， including the Self-rating Anxiety Scale （SAS）， the Self-rating Depression Scale （SDS）， and the Pittsburgh Sleep Quality Index （PSQI）， were administered for anxiety， depressive symptoms， and sleep quality， respectively. ResultsIn adolescent patients with emotional disorders， the SAS score exhibited significant positive correlations with brain load （r_s=0.328， P<0.01）， emotional stress （r_s=0.341， P<0.01）， and cerebral fatigue （r_s=0.286， P<0.01）. The SDS score was positively correlated with brain load （r_s=0.275， P<0.01）， emotional stress （r_s=0.241， P<0.05）， and cerebral fatigue （r_s=0.311， P<0.01）， while showing a significant negative correlation with cerebral vitality （r_s=-0.212， P<0.05）. Additionally， the PSQI total score demonstrated positive correlations with brain load （r_s=0.340， P<0.01）， emotional stress （r_s=0.322， P<0.01）， and cerebral fatigue （r_s=0.229， P<0.05）. ConclusionFrontal EEG-derived indices， including brain load， emotional stress， cerebral fatigue and cerebral vitality， may serve as objective markers for reflecting anxiety， depression， and sleep quality in adolescents with emotional disorders. ［Funded by Beijing High level Innovation and Entrepreneurship Talent Support Program （number， 202504841041）； Horizontal Joint Project］

Objective: To assess the status of sexual behaviors, HIV/AIDS knowledge awareness, and novel synthetic drug use among school attending young students in Guangdong Province, so as to provide evidence base for formulating targeted intervention strategies. Methods: From September to December 2024, a convenience sampling method was employed to conduct an anonymous online survey among 41 119 students from 20 higher education institutions and vocational colleges in Guangdong Province. Chi square test was utilized for rate comparisons and univariate analysis, and a multivariate Logistic regression model was applied to analyze factors associated with novel synthetic drug use. Results: The self reported rate of sexual behavior was 5.2%. Among sexually active students, the rates of unprotected sexual intercourse, having temporary sexual partners, and having commercial sexual partners were 32.4%, 34.5%, and 26.3%, respectively. The awareness rate of HIV related knowledge was 75.7%. The overall use rate of novel psychoactive substances(NPS) was 1.0%, and among sexually active students it was 6.5%. Multivariate Logistic regression analysis showed that students with sexual experience ( OR =4.15) and those with HIV testing history ( OR =9.38) had higher risks of NPS use; among sexually active students, those with unprotected sexual intercourse ( OR =6.83) and those with commercial sexual partners ( OR = 4.68 ) had higher risks of NPS use (all P <0.05). Conclusions The HIV/AIDS knowledge level among surveyed students needs further improvement, and high risk sexual behaviors are cross linked with novel synthetic drug use. It is recommended to carry out integrated health education for all students and implement comprehensive targeted interventions for sexually active students.

BackgroundStressful life events are associated with subclinical depressive and anxious symptoms， which may increase the risk of subsequent depressive and anxiety disorders. However， the mechanisms linking stressful life events to subclinical emotional symptoms remain unclear. ObjectiveTo explore the clinical characteristics of individuals with subclinical depression and anxiety following stressful events， and to analyze the mechanisms by which stressful events affect subclinical depressive and anxious symptoms， so as to provide a reference for the early identification and intervention of emotional symptoms in individuals under stress. MethodsFrom December 2024 to April 2025， 80 individuals with subclinical depression and/or anxiety （study group） and 80 healthy controls were recruited via the online official accounts of Beijing Anding Hospital， Capital Medical University and Beijing Huilongguan Hospital， Capital Medical University. Participants completed the Patients' Health Questionnaire Depression Scale-9 item （PHQ-9）， the Generalized Anxiety Disorder Scale-7 item （GAD-7）， the Life Event Scale （LES）， the Self-rating Idea of Suicide Scale （SIOSS）， and the Dysfunctional Attitude Scale （DAS）. Spearman rank correlation analysis was used to examine the associations in the study group. Serial mediation analyses were conducted using model 6 of Process version 4.1， to test whether cognitive distortion and hopelessness mediated the associations of stressful life events with subclinical depressive and anxious symptoms. ResultsCompared with healthy controls， participants with subclinical depressive and anxious symptoms had higher scores on PHQ-9， GAD-7， LES， SIOSS hopelessness subscale， and DAS scores （Z/t=10.294， 9.197， 4.659， 6.918， 3.517， P<0.01）. In the study group， GAD-7 score was positively correlated with LES， DAS， and SIOSS hopelessness subscale scores （r_s=0.233， 0.465， 0.588， P<0.05）； SIOSS hopelessness subscale score was positively correlated with DAS and LES scores （r_s=0.393， 0.309， P<0.01） and cognitive distortion was positively correlated with stressful life events（r_s=0.432， P<0.01）. Stressful life events were directly associated with subclinical anxiety symptoms （β=0.040， 95% CI： 0.015–0.065， P<0.05）， and showed a significant serial indirect association with subclinical anxiety symptoms （indirect effect=0.006， 95% CI： 0.001–0.017， P<0.01）， accounting for 7.15% of the total effect. Stressful life associated with subclinical depressive symptoms （β=0.087， 95% CI： 0.060–0.115， P<0.01）， however， the indirect effect through cognitive distortion and hopelessness were not statistically significant. ConclusionAfter experiencing stressful events， individuals with subclinical depression and anxiety exhibit more pronounced cognitive distortions and hopelessness. Stressful events can both directly affect subclinical anxiety symptoms and indirectly affect them through the serial mediating effects of cognitive distortion and hopelessness. Stressful events have a direct effect on subclinical depressive symptoms， whereas the mediating effects of cognitive distortion and hopelessness are no statistically significant. ［Funded by the Training Program for the Development of High-level Public Health Technical Talents （number， Academic Leader-01-22）； www.chictr.org.cn number， ChiCTR2400093516］

In September 2023， the Measures for Scientific and Technological Ethics Review （Trial Implementation） was issued， revising the provisions related to the simplified procedure for ethical review in Chapter 3， Section 3. This revision of these provisions provides systematic guarantees for further optimizing ethical review work， ensuring that ethical review procedure is well-regulated， and improving scientific research efficiency. The “simplified procedure” does not mean reducing the quality and requirements of the review. Instead， based on always following internationally recognized ethical standards and emphasizing not violating national laws and regulations， improving the efficiency of ethical review and subsequent research work， and promoting the development of life sciences and medical research involving humans. In practical work， it introduces numerous new opportunities and challenges for the improvement of ethics review ability， such as new tests on the judgment and decision-making power of ethics committees， how to ensure the reliability and controllability of the conditions related to the simplified review procedure， and how to determine the basic conditions for adopting the simplified review procedure for review. Therefore， to actively respond to the challenges and possible risks brought by the simplified procedure review， efforts should be made to achieve three “unifications”， including the unification of researchers’ moral autonomy and the heteronomy of supervision implemented by relevant departments； the unification of the standard formulation of the simplified procedure review and the review work in practice； and the unification of ethical responsibility and legal responsibility.

BACKGROUND:Rheumatoid arthritis is an inflammatory disease.Many studies have shown that wogonin has a good anti-inflammatory effect on rheumatoid arthritis,but its exact efficacy and specific mechanism of action remain to be clarified. OBJECTIVE:To investigate the mechanism of wogonin ameliorating joint inflammation by regulating endoplasmic reticulum stress pathway in rats with collagen-induced arthritis. METHODS:(1)At the animal level:Female Wistar rats were divided into healthy control group,arthritis model group and wogonin treatment group.Rat models of arthritis in the latter two groups were established by subcutaneous injection of bovine type Ⅱ collagen and adjuvant.In the wogonin group,wogonin was given by gavage for 28 consecutive days after modeling.During this period,the rats in each group were weighed,and arthritis score and ankle swelling were measured every 7 days.After the experiment,the pathological changes of the joint were observed,the mRNA and protein levels of endoplasmic reticulum stress pathway GRP78 and CHOP were detected by qRT-PCR,western blot,and immunohistochemistry.(2)At the cellular level,cell counting kit-8 was used to detect the cytotoxic effect of wogonin on fibroblast-like synoviocytes from rats with collagen-induced arthritis.The fibroblast-like synoviocytes induced by thapsigargin were treated with different concentrations of wogonin.The levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant were detected by ELISA,and the intracellular reactive oxygen species in each group were determined by DCFH-DA probe method.The mRNA and protein levels of GRP78,IRE1α,XBP1s and CHOP were detected by qRT-PCR and western blot,respectively. RESULTS AND CONCLUSION:Compared with the healthy control group,arthritis index score and ankle swelling degree in the arthritis model group were increased(P<0.01),synovial hyperplasia,inflammatory cell infiltration,cartilage destruction and bone erosion were observed in pathological sections,and the mRNA and protein expressions of GRP78 and CHOP in the ankle were significantly increased(P<0.01),which were mainly located in synovial tissue and articular surface.Compared with the arthritis model group,the arthritis index score and ankle swelling degree in the wogonin treatment group were decreased(P<0.05),synovial hyperplasia and the number of inflammatory cells were decreased,cartilage destruction and bone erosion were alleviated,the mRNA and protein expression levels of GRP78 and CHOP in the ankle were decreased(P<0.05),particularly in synovial tissue and on the articular surface.There was no significant difference in body mass among the three groups(P>0.05).In the cell experiment,200 μmol/L wogonin significantly reduced the survival rate of fibroblast-like synoviocytes(P<0.01).Compared with the blank control group,the levels of interleukin-1β,tumor necrosis factor-α,content of reactive oxygen species,and mRNA and protein expression of GRP78,IRE1α,XBP1s,and CHOP in the thapsigargin group were significantly increased(P<0.05);compared with the thapsigargin group,50 and 100 μmol/L wogonin significantly reduced the levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant(P<0.05,P<0.01),and 100 μmol/L wogonin significantly reduced the content of reactive oxygen species(P<0.01)and down-regulated the mRNA and protein expression levels of GRP78,IRE1α,XBP1s and CHOP(all P<0.05).These results suggest that wogonin can effectively alleviate joint inflammatory responses in rats with collagen-induced arthritis,and the endoplasmic reticulum stress pathway may be the key target of its intervention.

BACKGROUND:Our previous study found that Modified Erxian Pill could alleviate inflammation in collagen-induced arthritis rats,but its mechanism needs to be further verified. OBJECTIVE:To analyze the components absorbed in the blood of Modified Erxian Pill,and observe the effect of the drug-containing serum of Modified Erxian Pill on pyroptosis of J774A.1 macrophages. METHODS:(1)Analysis of components absorbed in the blood of Modified Erxian Pill:Ultra-high performance liquid chromatography-high resolution mass spectrometry was used to detect and identify Modified Erxian Pill and its components absorbed in the blood.(2)Effect of the drug-containing serum of Modified Erxian Pill on pyroptosis of J774A.1 macrophages:Molecular docking technology was used to initially verify the sesquiterpenoids and NLRP3 in components absorbed in the blood of Modified Erxian Pill.J774A.1 macrophages were randomly divided into blank control group,lipopolysaccharide+adenosine triphosphate group,and lipopolysaccharide+adenosine triphosphate+Modified Erxian Pill with low(2.5%),medium(5%),and high(10%)dose groups.The release of lactate dehydrogenase in the cell supernatant of each group was detected according to the kit instructions.The levels of interleukin-1β and interleukin-18 in cell supernatant were detected in each group by ELISA.The cell membrane damage was detected by Hoechst/PI staining.The expression levels of NLRP3,Caspase-1,GSDMD,and GSDMD-N protein in the cells of each group were detected by western blot assay. RESULTS AND CONCLUSION:(1)A total of 32 active components of Modified Erxian Pill were identified,and 21 components entered the blood.The main components into blood included a variety of sesquiterpenoids.(2)Molecular docking results showed that 3-O-Acetyl-13-deoxyphomenone,Incensol oxide,Atractylenolide III,Rupestonic acid,and 3,7-Dihydroxy-9,11-eremophiladien-8-one had good binding activity with NLRP3.(3)Compared with the blank control group,lactate dehydrogenase activity and the expression levels of interleukin-1β and interleukin-18 were significantly increased in cell supernatant of lipopolysaccharide+adenosine triphosphate group(P<0.001).Hoechst/PI staining showed that the number of PI-positive cells was significantly increased.After the intervention of lipopolysaccharide+adenosine triphosphate+Modified Erxian Pill group,all of them showed different degrees of reduction.(4)Compared with the blank control group,NLRP3,Caspase-1,GSDMD,and GSDMD-N protein expression levels were significantly increased in the lipopolysaccharide+adenosine triphosphate group(P<0.05).Compared with lipopolysaccharide+adenosine triphosphate group,the protein expressions of NLRP3,Caspase-1,GSDMD,and GSDMD-N were significantly decreased in the lipopolysaccharide+adenosine triphosphate+Modified Erxian Pill group(P<0.05),and had a certain dose dependence.These findings verify that the drug-containing serum of Modified Erxian Pill may inhibit the pyroptosis of J774A.1 macrophages by regulating the NLRP3/Caspase-1/GSDMD pathway.

Macrophages are central mediators of cardiac inflammation and are involved throughout the development of myocardial ischemia.Glucose metabolism reprogramming is an event that affects the core of macrophage polarization,and it can alter the phenotype of macrophages by regulating their glycolytic modes,which in turn affects myocardial injury-repair process.This study sorted out pathogenesis of"deficient qi stagnation"and the related study of macrophage polarization induced by glucose metabolism reprogramming,combined with the overall diagnosis and microscopic point of view,and proposed that myocardial ischemia lies in the cardiac collaterals and the accumulation of pathological products due to abnormal reprogramming of macrophage glucose metabolism in the pathogenesis of myocardial ischemia,which is similar to TCM theory of"deficient qi stagnation".The increase of inflammatory factors in myocardial ischemia and the outcome of ventricular remodeling caused by macrophage polarization imbalance can be regarded as the"toxic damage"process of heart.In the clinical practice,the method of"supporting the healthy qi and replenishing the deficiency,and eliminating the stagnation and detoxification"is used to improve the reprogramming of glucose metabolism,remodel the polarization of macrophages,reduce the inflammatory reaction,and delay the progression of the disease.Therefore,the use of TCM therapy to regulate glucose metabolism reprogramming to induce macrophage polarization is expected to bring new therapeutic ideas for myocardial ischemia.